Objective: To explore whether T lymphocytes subgroup, B lymphocytes, platelet antigen CD41a, CD61 or platelet antibodies are involved in the platelet transfusion refractoriness.
Methods: Forty-seven patients diagnosed as platelet transfusion refractoriness and 32 patients that achieved effective platelet therapy were ennolled in this study. Flow cytometry was performed to detect the proportion of cytotoxic T cell (CD3(+)CD4(-)CD8(+)), helper T cell (CD3(+)CD4(+)CD8(-)) and B lymphocytes (CD19 (+) ), and the expression of platelet glycoproteins, including CD41a and CD61, while platelet antibodies were also measured by solid-phase agglutination.
Results: The significant lower level of helper T cell (36.60% vs 48.53%), higher level of cytotoxic T cell (53.26% vs 44.02%) and lower cytotoxic/helper T cell ratio (0.85 vs 1.31) were observed in platelet refractoriness group when compared with effective platelet therapy group (P<0.05). However, the significant difference was not observed in B lymphocytes between the two group (3.02% vs 2.85%, P>0.05). Platelet glycoproteins CD41a and CD61 and antibodies were both expressed at high levels in platelet refractoriness group (88.10% vs 51.69%, 88.36% vs 51.83%, 85.37% vs 14.82%, respectively, P<0.05).
Conclusions: Activation of cytotoxic T cells, suppression of helper T cells, higher expression level of platelet glycoproteins CD41a and CD61 as well as the development of anti-platelet antibodies are involved in the immunologic mechanism of platelet refractoriness.
目的: 探讨T、B淋巴细胞，血小板膜糖蛋白和血小板抗体在血小板输注无效中作用。
方法: 选择41例临床确诊血小板输注无效患者为研究对象，以27例血小板输注有效患者为对照组，采用流式细胞术检测两组患者外周血细胞毒性T淋巴细胞（CD3 +CD4−CD8+）、辅助性T淋巴细胞（CD3 + CD4+CD8−）、B淋巴细胞（CD19+）比例和血小板膜糖蛋白CD41а、CD61的表达，采用固相凝集法检测两组患者血清中的血小板抗体。
结果: 与对照组比较，血小板输注无效组患者：①辅助性T细胞比例明显下降（36.60%对48.53%），细胞毒性T细胞比例显著增高（53.26%对44.02%），二者比值下降（0.85对1.31），差异均有统计学意义（P值均<0.05）；②B淋巴细胞比例差异无统计学意义（3.02%对2.85%，P=0.901）；③CD41а阳性细胞率[（88.10±12.75）%对（51.69±24.45）%，P=0.001]和CD61阳性细胞率[（88.36±12.31）%对（51.83±24.48）%，P<0.001]均显著升高；④血小板抗体阳性率显著增高（85.37%对14.82%，P<0.05）。
结论: 细胞毒性T淋巴细胞的激活、辅助性T细胞的抑制、血小板膜糖蛋白CD41а和CD61的表达以及血小板抗体的产生均在血小板输注无效的发生过程中发挥重要作用。